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Background  The bone-bone marrow interface is an area of the bone marrow microenvironment in which both bone remodeling cells, osteoblasts and osteoclasts, and hematopoietic cells are anatomically juxtaposed. The close proximity of these cells naturally suggests that they interact with one another, but these interactions are just beginning to be characterized.    Methodology/Principal Findings  An  Id1 −/−   mouse model was used to assess the role of Id1 in the bone marrow microenvironment. Micro-computed tomography and fracture tests showed that  Id1 −/−   mice have reduced bone mass and increased bone fragility, consistent with an osteoporotic phenotype. Osteoclastogenesis and pit formation assays revealed that loss of  Id1  increased osteoclast differentiation and resorption activity, both  in vivo  and  in vitro , suggesting a cell autonomous role for Id1 as a negative regulator of osteoclast differentiation. Examination by flow cytometry of the hematopoietic compartment of Id1  −/−   mice showed an increase in myeloid differentiation. Additionally, we found increased expression of osteoclast genes,  TRAP ,  Oscar , and  CTSK  in the  Id1 −/−   bone marrow microenvironment. Lastly, transplantation of wild-type bone marrow into  Id1 −/−   mice repressed  TRAP ,  Oscar , and  CTSK  expression and activity and rescued the hematopoietic and bone phenotype in these mice.    Conclusions/Significance  In conclusion, we demonstrate an osteoporotic phenotype in  Id1 −/−   mice and a mechanism for Id1 transcriptional control of osteoclast-associated genes. Our results identify  Id1  as a principal player responsible for the dynamic cross-talk between bone and bone marrow hematopoietic cells.

Id1 Represses Osteoclast-Dependent Transcription and Affects Bone Formation and Hematopoiesis